Copyright 2006 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2006
An 82-year-old woman presented to the emergency department with altered mental status. Her son had conversed with her by telephone 36 hours before the onset, but he could not reach her by telephone 24 hours after that. She had a medical history of right hemiparesis and dysarthria 14 years earlier and had been taking medication for hypertension as well as aspirin. She was diagnosed as having type 1 diabetes mellitus and began taking medication for her diabetes 1 month prior to this onset. Her blood glucose level during the emergency department visit was 12 mg/dL (0.7 mmol/L). Her initial blood pressure was 173/76 mm Hg and oxygen saturation was 91.3%. Diffusion-weighted magnetic resonance (MR) imaging and T2-weighted MR imaging showed diffuse cortical high signal (Figure). The brainstem, cerebellum, and thalamus were spared.1 Despite prolonged hypoglycemia, the dorsofrontal cortex and occipital poles were also spared. The signal changes on the hippocampus were relatively small. On T2-weighted MR imaging, a focal high-signal lesion was seen in the thalamus bilaterally (with more prominence on the left side) and in the centrum semiovale. Diffuse white matter lesions were seen on T2-weighted MR imaging. Considering her medical history and the diffusion-weighted MR image, it seems more likely we were looking at an old ischemic lesion and hypertensive change. She died 3 days after hospital admission. Diffusion-weighted MR imaging may help differentiate acute hypoglycemic lesions from old ischemic lesions and diffuse white matter changes. Unlike hypoxic damage, the occipital cortex, dorsofrontal cortex, and hippocampus may be more resistant to prolonged hypoglycemia.
Cho S, Minn Y, Kwon K. Severe Hypoglycemia and Vulnerability of the Brain. Arch Neurol. 2006;63(1):138. doi:10.1001/archneur.63.1.138